Weitere Antikörper gegen SOX9 Interaktionspartner

Human SRY (Sex Determining Region Y)-Box 9 (SOX9) Interaktionspartner

These results unravel NEDD9 as a common target for SOX10 or high SOX9 to partly mediate their oncogenic events, and most importantly, reconcile previous discrepancies that suboptimal level of SOX9 expression is anti-metastatic whereas high level of SOX9 is metastatic in a heterogeneous population of melanoma.

Our data uncover the ZEB1/ERalpha-miR-190-SOX9 axis and suggest a mechanism by which the Wnt/beta-catenin signaling pathway is involved in breast cancer anti-estrogen therapy.

SOX9 was upregulated in breast cancer (BC) tissues and its expression was inversely correlated with that of miR511. Furthermore, SOX9 inhibition simulated the tumorsuppressive roles of miR511 overexpression in BC cells, while SOX9 reintroduction partially rescued these effects of miR511. Notably, the upregulation of miR511 targeted SOX9 to deactivate the PI3K/Akt signaling in BC in vitro and in vivo.

SOX9 polymorphism rs1042667 shows significant association with the occurrence of osteoarthritis (OA) in Chinese Han population, but not rs12601701. Furthermore, the interaction between the polymorphisms rs12601701 and rs1042667 is suggested to contribute to the risk of OA as well.

The present study identified Scmlike with four malignant brain tumor domains 2 (SFMBT2) as a novel regulator of SOX9 expression.

Isolate living subpopulations of duct cells enriched for high or low expression of HNF1beta and SOX9.

This is the first report of molecularly confirmed maternal germinal mosaicism for a SOX9 mutation. We suggest that a meticulous clinical examination of the parents, even if they are superficially healthy, is needed to avoid overlooking germinal mosaicism of SOX9 mutations.

Our study tested and verified that MALAT1 was highly expressed in colorectal cancer tissues and cells. MALAT1 regulated miR-145 expression as a competing endogenous RNA, and down-regulation of MALAT1 suppressed proliferation and invasion, promoted cell cycle G1 phase and apoptosis of cancerous cells by increasing the expression of miR-145 and decreasing SOX9 expression.

Human sex reversal is caused by duplication or deletion of core enhancers upstream of SOX9.

Our study demonstrated that Reg IV positively regulates the expression of SOX9 and is involved in tumor cell invasion and migration in gastric cancer.

SOX9 may be involved in the tumorigenesis and progression of oral squamous cell carcinoma (OSCC). Furthermore, its cytoplasmic expression represents a potential predictive biomarker for tumor aggressiveness and OSCC prognosis.

This is supported by the fact that ECG correlates with the expression of SOX9 indicating that this biomarker probably plays an important role in the pathogenesis of gastric cancer and ECG formation.

role in regulation of extracellular matrix balance, the inflammatory process, and the immune response of inflamed dental pulp

Study found a positive relationship between LINC00052 and miR-101-3p, and a negative relationship between miR-101-3p and SOX9 in hepatocellular carcinoma (HCC) tissues. Besides, miR-101-3p was involved in LINC00052 inhibiting HCC cells proliferation and metastasis. At the molecular level, LINC00052 downgulated SOX9 to inhibit HCC cells proliferation and metastasis by interacting with miR-101-3p.

SOX9 expression is related to prognosis in patients with oesophageal squamous cell carcinoma, although it is not an independent prognostic factor.

High expression of SOX9 can promote the migration and lymph node metastasis of oral squamous cell carcinoma

Irx3 is a novel chondrogenic factor of mesenchymal cells, which acts synergistically with Bmp2-mediated signaling, and regulates chondrogenesis independent of the transcriptional machinery associated with Sox9-mediated regulation.

During embryogenesis, SOX9-positive (+) cells inside hair follicles, which were previously known to give rise to hair follicle stem cells (HFSCs) and cells of the hair follicle lineage, can also give rise to Merkel Cells. Interestingly, while SOX9 is critical for HFSC specification, it is dispensable for Merkel cell formation. Conversely, FGFR2 is required for Merkel cell formation but is dispensable for HFSCs.

These results suggest that targeting SOX9 is a viable strategy to promote reparative axonal sprouting, neuroprotection and recovery after stroke.

a novel regulatory relationship between the retinal pigmented epithelium (RPE) transcription factors Pax6 and Sox9 that controls the timing of RPE differentiation and the adjacent choroid maturation, is reported.

enhancer 13, a 557-base pair element located 565 kilobases 5' from the transcriptional start site, is essential to initiate mouse testis development; its deletion results in XY females with Sox9 transcript levels equivalent to those in XX gonads.

These results indicate that THRAP3 negatively regulates SOX9 transcriptional activity as a cofactor of a SOX9 transcriptional complex during chondrogenesis.

Sox9 is identified as important factor of VSMC function by modulation the extracellular matrix composition and calcium deposition, which are important processes in plaque development.

these findings widen our current knowledge of SOX9 targets in early chondrogenesis and call for new studies to identify the pioneer and transactivating factors that act upstream of or along with SOX9 to prompt chromatin remodeling and specific gene activation at the onset of chondrogenesis and other processes.

The data support a model of SOX9-GLI-FOXA phasic gene regulatory network in chondrocyte development. Together, SOX9-GLI auto-regulate and cooperate to activate and repress genes in proliferating chondrocytes. Upon hypertrophy, FOXA competes with SOX9, and control toward terminal differentiation passes to FOXA, RUNX, AP1 and MEF2 factors.

Ctgf is the direct target gene of SOX9 in chondrocytes and nucleus pulposus cells.

The patterns of SRY/SOX9 expression associated with the process of gonadal morphogenesis in rabbit appear similar to those of other mammals, including humans.

SOX9 Antigen-Profil

Beschreibung des Gens

The protein encoded by this gene recognizes the sequence CCTTGAG along with other members of the HMG-box class DNA-binding proteins. It acts during chondrocyte differentiation and, with steroidogenic factor 1, regulates transcription of the anti-Muellerian hormone (AMH) gene. Deficiencies lead to the skeletal malformation syndrome campomelic dysplasia, frequently with sex reversal.